30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The crucial role of the cholinesterases in neural transmission makes them a primary target of a large number of cholinesterase-inhibiting drugs and toxins. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evidence exists for both cholinergic and glutamatergic involvement in the etiology of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
AChE-selective inhibitors and a dual AChE and BuChE inhibitor demonstrate symptomatic efficacy in AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A design strategy to convert a dual-binding site AChE inhibitor into triple functional compounds with promising in vitro profile against multifactorial syndromes, such as Alzheimer's disease, is proposed. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The therapeutic arsenal for the treatment of Alzheimer's disease (AD) remains confined to a group of four inhibitors of AChE and one NMDA receptor antagonist, which are used to provide a relief of the very late symptoms of the dementia, i.e. the cognitive and functional decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent phase 3 clinical trials have shown that memantine is effective in the treatment of both mild and moderate-to-severe Alzheimer's disease and possibly vascular dementia (multi-infarct dementia). 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Disruption of axonal transport is a hallmark of several neurodegenerative diseases, including Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta (Aβ) oligomers accumulate in the brain tissue of Alzheimer disease patients and are related to disease pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological processes of neurodegenerative disorders such as Alzheimer's and Parkinson's diseases engender synaptic and neuronal cell damage. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinesterase inhibitors have produced the best evidence of clinical efficacy for treating patients with Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A new family of multitarget molecules able to interact with acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), as well as with monoamino oxidase (MAO) A and B, has been synthesized. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The therapeutic approach for improving the cognitive function in patients with Alzheimer's disease (AD) is mainly based on the potentiation of central cholinergic activity and is achieved clinically by the use of acetylcholinesterase (AChE) inhibitors such as tacrine, donepezil, rivastigmine, galantamine and other drugs currently in clinical trials. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pharmacological inhibition of excitatory amino acid neurotransmission has evolved to be a major topic in neuropharmacology since enhanced synaptic action of glutamate and possibly other related neurotransmitters has been suggested to play a role both in acute neurological conditions such as ischemia and epilepsy and in chronic degenerative neurological diseases including Parkinson's disease, Huntington's disease and Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Donepezil hydrochloride is the most widely prescribed drug for Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From a public health viewpoint, recognition of VCI before the development of dementia and correction of vascular burden on the brain may lead to a global decrease of incident dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Calcium homeostasis plays a major role in maintaining neuronal function under physiological conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the year 1999, a vaccine approach was found to reduce amyloid deposits in transgenic mice overproducing the amyloid precursor protein. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies that alleles in the hemochromatosis gene may accelerate the onset of Alzheimer's disease by five years have validated interest in the model in which metals (particularly iron) accelerate disease course. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Calcium homeostasis plays a major role in maintaining neuronal function under physiological conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
With each failure of anti-amyloid-β therapy in clinical trials, new trials are initiated with no hint of slowing down. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The exact mechanisms leading to Alzheimer's disease (AD) are largely unknown, limiting the identification of effective disease-modifying therapies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The properties of S. miltiorrhiza indicate their therapeutic potential in AD via multiple mechanisms. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta protein (Abeta) levels are elevated in the brain of Alzheimer's disease patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Family physicians play a crucial role in the management and ongoing care of patients with Alzheimer disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Imaging agents capable of assessing amyloid-beta (Abeta) content in vivo in the brains of Alzheimer's disease (AD) subjects likely will be important as diagnostic agents to detect Abeta plaques in the brain as well as to help test the amyloid cascade hypothesis of AD and as an aid to assess the efficacy of anti-amyloid therapeutics currently under development and in clinical trials. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 30,980 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,042 records (3.4% of the library) are not peer-reviewed — 967 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events